Methods for compositions for reducing or eliminating symptoms of withdrawal from drugs and alcohol

ABSTRACT

Methods and compositions of reducing or eliminating the symptoms of withdrawal from drug or alcohol in drug or alcohol-dependent persons, while restoring the patient to nutritional health. The methods including parenteral administration of solutions containing high doses of ascorbic acid; while the compositions of the invention comprise at least about 20% (w), or at least about 25% (w), or at least about 30% (w), or at least about 35% (w), or at least about 38% (w) of ascorbic acid and a local anesthetic.

RELATED APPLICATIONS

This is a continuation of U.S. patent application Ser. No. 16/530,602,filed Aug. 2, 2019, which was a continuation of U.S. patent applicationSer. No. 16/117,648, filed Aug. 30, 2018, each of which is herebyindividually incorporated by reference herein.

FIELD OF THE INVENTION

This invention is drawn to compositions and methods pertaining to atreatment for reducing or eliminating the physical symptoms ofwithdrawal from substances of abuse (SOA), such as habit-forming drugsand alcohol. The described methods and compositions are capable ofreducing or totally and rapidly detoxifying the subject while inhibitingor reducing manifestation of withdrawal symptoms and eliminating theintense physiological/psychological craving for the SOA. At the sametime, the present methods and compositions restore and rebuild thenutritional health of the patient.

BACKGROUND OF THE INVENTION

Drug addiction and alcoholism are serious personal, social and economicproblems. Particularly in view of the current opioid epidemic, addictiveopioid drugs such as heroin, morphine, oxycontin, methadone,buprenorphine, fentanyl, etc., as well as addictive non-opioid drugsincluding cocaine, barbiturates, benzodiazepines, methamphetamine, areabused in the United States at record rates. Addition to SOAs exacts aterrible price in suffering, overdoses, and a high financial cost, tosociety as a whole.

Among all SOAs, alcohol addiction is the number one killer, beingresponsible for 88,000 deaths per year in the United States, accordingto the National Institutes of Health; all other drugs (illicit andprescription) combined resulted in 64,000 overdose deaths per year inthe U.S. in 2017.

Vast sums of money are spent in treatment and rehabilitation programs inan effort to treat drug addition and alcoholism and return the addict tohealth. As illicit drugs tend to be expensive, it is not uncommon for anaddict to engage in criminal enterprises, such as robbery or theft, toobtain the money necessary to support his or her drug habits. Accordingto the National Institute of Alcohol Abuse and Alcoholism the estimatedannual cost of alcohol abuse alone in the U.S. as of 2010 was $249billon dollars. When the costs of drug abuse (including tobacco andprescription drug misuse) are included, the total annual economic costof drug and alcohol abuse increased to more than $750 billion dollarsper year.

Current approaches to heroin and other opioid addiction include“maintenance” programs using opioid heroin analogs such as methadone andbuprenorphine as a substitute for the illicit narcotic, such as heroin.Under such maintenance programs, the patient continues to be addicted tothe analog (which is usually less potent as an intoxicant than the SOA)until or unless the patient wishes to taper off the analog. These analogcompounds may be combined with the opioid receptor antagonist naloxone(sold under the trade name Narcan®) to prevent misuse of the“substitute”. Thus, these maintenance methods are self-defeating becausemethadone and buprenorphine, while less intoxicating on a molar basisthan heroin, are themselves addicting. Such maintenance methodstherefore merely substitute an illegal form of drug addiction foranother, legal form; the patient remains addicted to drugs. Moreover,the analogs themselves may be abused or combined with other drugs,resulting in overdose and death. In 2004 methadone contributed to 3.849deaths in 2004; in most cases in combination with other drugs,especially benzodiazapines.

Another approach to opioid addiction is “cold turkey” withdrawal, wherethe addict refrains from ingesting the SOA. Tus may be done voluntarily,but is more often that the patient is either physically restrained fromusing the drug, or placed within a drug rehabilitation facility as acondition of probation or parole. Withdrawal from opiates ischaracterized by severe muscle spasms, chills, lacrimation, depression,anxiety, digestive problems, diarrhea, fatigue, vomiting, and acontinuing physical craving for the narcotic. The “cold turkey” methodinvolves a not inconsiderable amount of pain and for this reason isdreaded and avoided by addicts.

Withdrawal from opiates alone does not usually involve seizures or arisk of death. However, withdrawal from certain other drugs (such asbenzodiazepines, barbiturates and alcohol) can result in grand madseizures and an increased risk of death without medical intervention.

A further method of drug detoxification has been the use of drugs suchas sedatives (e.g., Valium (diaxepam) and other benzodiazepines), andanalgesics (such as Darvon (propoxyphene, an opioid now banned by theFDA due to serious side effects) to attempt to reduce the patient'swithdrawal symptoms from the offending drug.

Alcohol withdrawal may range in severity from mild tremors toconvulsions, delirium tremens (DTs) and death. Such symptoms typicallybegin to occur between 6 and 48 hours after heavy alcohol consumptiondecreases.

Various methods are used to wean an alcoholic from dependency onalcohol. Current approaches to alcoholism may include the administrationof doses of alcohol to the patient (“alcohol loading”) to inducesickness, after which unpleasant confrontations are initiated tostimulate aversion to drinking.

There is also the electrode method of stimulus-response to createaversion. An alcoholic is given a drink and as the drink is raised tothe lips he or she receives an uncomfortable electric stimulus in orderto create an aversion to drinking.

In chemical variations of this method, the initially detoxed patient isgiven a daily dose of an acetaldehyde dehydrogenase inhibitor such asdisulfiram (sold under the trade name “Antabuse®”). After ingestingdisulfiram when even small amounts of alcohol are consumed the patientmay experience “hangover” symptoms such as flushing, throbbing in headand neck, throbbing headache, respiratory difficulty, nausea, copiousvomiting, sweating, thirst, chest pain, palpitation, dyspnea,hyperventilation, tachycardia, hypotension, syncope, marked uneasiness,weakness, vertigo, blurred vision, and confusion. Severe reactionscaused, for example, by ingestion of large amounts of alcohol may resultin death.

Cold turkey detoxification from alcohol is discouraged at least in casesof moderate to severe alcohol withdrawal due to the risk of seriousadverse reactions or death.

All the above approaches, and others known to date, treat alcoholism ordrug addiction as a problem to be treated essentially by preventingaccess to, and ingestion of, the offending substance. All these methodsrequire anywhere from 72 hours to 21 days, with accompanying withdrawalsymptoms, to accomplish detoxification, which is a slow and painfulprocess. While sedatives can ease anxiety, none of these methodssignificantly reduce either withdrawal symptoms or the continuingcraving for the addictive substance.

Although electrolyte balance is currently addressed in the treatment ofalcohol withdrawal, only slight attention, if any, is directed toward apatient's overall nutritional health or lack thereof when withdrawingfrom addictive substances.

Libby, A. & Stone, THE HYPOASCORBEMIA-KWASHIORKOR APPROACH TO DRUGADDICTION THERAPY: A PILOT STUDY, (Lecture Presented at the WesternRegional Seminar of the International Academy of Preventive Medicine.San Francisco, Calif. (Jul. 16, 1977) presents theory and study dataconcerning the use of Vitamin C and the 20 essential amino acids in thetreatment of addiction.

Libby, U.S. Pat. No. 4,500,515, describes a method and composition fordetoxifying from addicts and alcoholics using about 10 g to about 15 gsodium ascorbate. The method comprises administering high oral doses ofsodium ascorbate until the patient experiences diarrhea, and thenswitching to parenteral administration of the remainder of a criticaltotal blocking dose of 28 to 35 grams of sodium ascorbate in a first dayof treatment.

Lines, U.S. Pat. No. 8,044,096, discloses a method for treating additionusing a combination of Vitamin C, Vitamin B₃ and quercetin n specificweight ratios.

All patents, patent publications and non-patent publications citedherein are hereby individually incorporated herein by reference in theirentirety. No admission is hereby made that any such reference is priorart to the present invention.

There is therefore need for a method for rapidly detoxifying drug and/oralcohol addicts that also effectively blocks withdrawal symptoms,reduces or eliminates the physical craving effect, and quickly returnsthe patient to a greater level of nutritional health, with a minimum ofinterruption in employment and other activities of daily life.

SUMMARILY OF THE INVENTION

The present patent application is drawn to methods and compositions forthe treatment of drug and/or alcohol dependency, including addiction toopioids such as heroin, morphine, oxycontin, methadone, buprenorphine,fentanyl, etc., as well as addictive non-opioid drugs including cocaine,barbiturates, benzodiazepines, methamphetamine, nicotine and alcoholdependency, which addresses the symptoms of substance abuse andwithdrawal as a metabolic problem. In its most complete aspects, themethod addresses detoxification, elimination of withdrawal symptoms, andrehabilitation.

Although not intending to be limited by theory. Applicant believes thatchronic drug and alcohol dependencies result in, and may be exacerbatedby, a general and severe lack of nutritional health, such that patientshow signs similar to those seen in people suffering from Kwashiorkor(severe protein-calorie malnutrition) and scurvy (Vitamin C deficiency).The applicant has also found that withdrawal symptoms from SOAs,including severe cravings, can be reduced or eliminated by quicklyrestoring nutritional health to the patient by the use of methodsinvolving the sequential parenteral administration of two or moreapplications containing different concentrations of ascorbic acid, withother vitamins, minerals, amino acids, and electrolytes.

In addition to providing nutrients, the present methods also involve theuse of compositions, such as compositions containing nutrients,vitamins, anti-oxidants and/or methylation-promoting agents, thatnourish the alcoholic's and addict's usually malnourished body andremove toxic oxidized compounds and free radicals from the body, ortarget such compounds and free radicals for excretion by the body. Theseprocesses of restoring nutritional health and eliminating metabolicwaste from the body.

Although not intending to be limited by theory, Application believesthat drugs and alcohol enter and leave to body in four stages:

1) absorption by the body depends on how the drug is administered. Drugsadministered orally—by eating, drinking, or swallowing pills—areabsorbed through the stomach and small intestine. Oral administration isby tar the predominant mode of alcohol use. The drug then passes throughthe liver before entering the bloodstream. Substances administered thisway take effect more slowly than drugs taken via other routes, such assmoking or injection.

Injection is one of the fastest ways for SOAs to reach body tissues andorgans through the bloodstream. Injection into the vein—or intravenousinjection—delivers the substance directly into the bloodstream.Injection into the muscle allows the substance to be absorbed into thebloodstream through the muscle tissue, and this is called anintramuscular injection. A subcutaneous injection is an injection intothe fatty tissue underneath the skin, which enables the substance to beabsorbed through the fatty tissue into the bloodstream. An intradermalinjection is an injection into the skin tissue.

Transdermal administration of illicit drugs is not as common as oraladministration or injection. Substances that are administered this wayare applied to the skin and then absorbed into the body. Once the drugis absorbed through the skin, it enters the bloodstream to be carriedthroughout the body and possibly to the brain.

Some drugs can be inhaled as gases. Gases penetrate the lining of thelungs very quickly, which allows the drug to enter the bloodstream.

Nasal inhalation of crushed drugs causes them to be absorbed through theblood vessels in the nose where they enter the blood stream. This issimilar to how buccal and sublingual drugs are absorbed. Buccal drugsare placed between a person's gums and cheek, and sublingual drugs areplaced under a person's tongue. Buccal and sublingual drugs dissolve inthe mouth and are absorbed through the tissue in the mouth to enter thebloodstream.

2) Distribution occurs via the body's circulatory system. Once an SOAhas entered the bloodstream, the heart pumps the blood throughout thebody, eventually carrying the substance to the brain.

Before a drug can enter the central nervous system it must pass throughthe blood-brain barrier, a system of tightly woven capillaries, that actas a barrier to prevent blood-borne pathogens and poisons from reachingthe brain. Some drugs that are intended to act on the central nervoussystem are specially designed to pass through this barrier other drugssimply app-r to have the ability to pass through the blood-brain barrierinnately.

Once the SOA has reached the brain, it can have various effects,including inducing euphoria or the “high” that is commonly associatedwith SOA use. SOAs accomplish this by affecting the neurotransmittersand neuroreceptors within the brain. Alcohol and many drugs affectdopamine levels, which results in feelings of pleasure and reward.

The act of distribution is also responsible for the many negative sideeffects that drugs can have on the body. Because substances are carriedto the entire body through the blood, they can have many unintendedeffects on the heart, liver, stomach, lungs, and/or other internalorgans.

3) Metabolism: Once a drug has been distributed throughout the body, itis broken down or metabolized. The amount of time a drug stays in thebody before being broken down varies between substances and methods ofadministration. AU substances that enter the bloodstream, regardless ofhow they are administered, are eventually carried to the liver to bemetabolized. Although the liver is the primary site of drug metabolism,drug metabolism may also occur in various other tissues and organs, suchas the kidneys, lungs, skin, and other sites.

The liver metabolizes SOAs through its enzymes, which break down thedrugs, while attempting to obtain energy from the metabolic process. Inso doing, the SOA is transformed into substances that can be easilyexpelled by the body, typically through the breath, urine or feces. Somedrugs, however, produce metabolites that have deleterious effects on thebody. Most SOAs (e.g. alcohol, amphetamines, opiates andbenzodiazepines) promote the generation of reactive oxygen species suchas free radicals. Reactive oxygen species (ROS) are small, highlyreactive, oxygen-containing molecules that are naturally generated insmall amounts during the body's metabolic reactions and can react withand damage complex cellular molecules such as fats, proteins, or DNA,thereby interfering with the body's normal defense mechanisms againstthese compounds through numerous processes. Alcohol produces deleteriousROS effects particularly in liver tissue, while opioids and amphetaminesproduce deleterious ROS effects in the brain and in intracellularorganelles such as the mitochondria. The metabolism of benzodiazepinesalso produce ROS effects in the brain and in intracellular organellessuch as the mitochondria and in DNA.

4) Finally, the last phase of a SOA within the body is excretion. Thisis the process by which the SOA exits the body, primarily via urine orfeces. The metabolized drug travels from the liver to the bladder andlarge intestine, where waste products carry what is left of the drug outof the body. Additionally, some waste products are transported to thelungs and excreted as a gas.

The reaction of ROS with antioxidants, or through the restoration ofvitamins and minerals that help the body remove or inactivate ROSconstitutes an important part of portion of the detoxification of thepresent invention.

The detoxification methods, systems, and compositions of the presentinvention provide for the substantial removal of intoxicants from thebody of a human suffering from alcohol dependency or drugs of abusewithin about 4-7 hours after commencing the parenteral administration ofthe compositions, and with little or none of the common symptoms of drugor alcohol withdrawal. This is true without regard to whether thepatient is drug or alcohol-free when the parenteral treatment iscommenced, or not. Continued treatment in accordance with the methodsand compositions of the invention continues to restore the body tohealth and to reduce or eliminate the physical and/r psychologicalsymptoms of withdrawal.

Ascorbic Acid

The compositions of the present invention comprise a treatment regimencomprising the use of high doses of Vitamin C, along with high doses ofB vitamins, minerals, methylation agents, anti-oxidants and certainamino acids at prescribed rates of administration. Preferably, themethod involves the parenteral application of aqueous compositionscontaining at least two different concentrations of ascorbic acid (or anwater soluble ascorbate salt), at least one of said compositionscomprising a antioxidative dose of ascorbic acid at a concentration insaid composition close to, but less than, saturation.

Without wishing to be limited by theory, it is believed that ascorbicacid can inhibit the analgesic activity of morphine by binding to opioidreceptors, such as the opioid p receptor.

Ketamine and ascorbic acid share anti-depressive activity, and thisappears to be modulated through the GABA_(A) and GABA_(B) receptors. Theanti-depressive activity of both agents act synergistically with aGABA_(A) receptor agonist, and are blocked by a GABA_(B) receptoragonist. Rosa, et al., Pharmacological Reports Vol 68, Issue 5 9%-1001(October 2016

When rats are permitted to self-administer morphine for 2 hours per dayon 10 consecutive days, then injected intraperitoneally with ascorbicacid, the level of self-administration (i.e. the number of leverpressings) and number an intensity of withdrawal symptoms decrease. SeeAlai et al., Pathophysiology. Vol. 12, No. 2, 103-107 (September 2005).

In studies of morphine-induced withdrawal syndrome after morphinecessation, is has been found that nitric oxide synthase (NOS) andphospholipase A2 may increase free radicals, and that inhibitors ofthese enzymes and free radical scavengers (e.g. anti-oxidants such asVitamin C) may attenuate withdrawal symptoms. See e.g., Mori, T., Behav.Pharmacol. 18(8) 725-9 (December, 2007). Interestingly, Ascorbic acidalso acts as a pro-oxidant at high concentrations under physiologicalconditions. Ascorbic acid's pro-oxidation activity arises as part of adose-dependent bimodal Activity, from its routine antioxidant propertyto generate free radicals at concentrations from 3-5 mM in vitro and0.5-about 2 mM ex vivo in humans.

The liver enzyme L-gluconolactone oxidase is the final enzyme in apathway of enzymes utilized by the mammalian liver to synthesizeascorbic acid from glucose. This biosynthesis of ascorbic acid is aconserved, vital and basic synthetic pathway occurring in nearly allliving organisms, both plant and animal.

However, in the course of evolution a primate ancestor of man suffered aconditional lethal mutation on the site of the gene controlling theproduction of the enzyme L-gluconolactone oxidase, destroying itsability to produce an active enzyme, and thus all its progeny from beingable to synthesize ascorbic acid. Among mammals only man, certainmonkeys, guinea pigs, and an Indian fruit eating bat (Pteropus medius)are unable to produce ascorbic acid in their livers. These few speciesare the only mammals that can contract and die of scurvy if deprived ofexogenous ascorbic acid.

Hippocrates was the tint to document that scurvy is a disease. Since the15^(th) century it has been known that citrus fruit would cure scurvy;however, this knowledge has been lost and repined continually throughhistory. For example, during the Age of Exploration (between 1500 and1800), it has been estimated that scurvy killed at least two millionsailors.

The Nobel Prize-winning biochemist Linus Pauling, extrapolating from therate of Vitamin C synthesis in rats of about 26-58 mg/day×kg, andassuming proportionality to both species and body weight, estimated thatthe optimal rite of intake of Vitamin C in man would be about 2 g toabout 3 g per day under normal circumstances if the L-gluconolactoneoxidase gene was not inactivated by mutation. When a person as understress (e.g., when infected by a common cold virus), this optimum amountmay increase significantly.

Ascorbic acid is concentrated in the brain, which is responsible for 25%of total glucose utilization. Such high activity correlates with a highoxidative metabolism requiring high levels of antioxidants forprotection against pathological conditions. Under normal brain activityascorbic acid, sequestered in glial reservoirs, is released to thesynaptic cleft, wherein it is taken up by neurons to scavenge reactiveoxygen species (ROS) generated during synaptic activity and neuronalmetabolism. In this process ascorbic acid is oxidized to dehydroascorbicacid, and released into the extracellular space, where it can berecycled by astrocytes.

When orally administered, the amount of ascorbic acid that can beadministered s limited by its laxative activity within the GI tract.Oral doses of up to about 2-5 g of Vitamin C at one time will normallycause diarrhea. The FDA recommended daily dose for an adult is 40 mg perday.

Previous attempts at Vitamin C-mediated detoxification methods emphasizethe necessity for the oral administration of relatively large doses ofascorbic acid, such as about 4 to 8 grams of ascorbic acid every 2hours, for a total of six hours or until the patient experiencesdiarrhea. See e.g., Libby, U.S. Pat. No. 4,500,515, col 2, lines 55-60.These prior methods indicate that diarrhea must be stimulated because itis “believe[d] to be absolutely necessary in order to decontaminate thebody, as well as [to] reinitiate normal peristalsis of the bowel.” Libbyet al., ORTHOMOLECULAR PSYCHIATRY, Vol. 11, No. 4, 277 (1982) at 282(emphasis in original).

By contrast, in the present application the applicant finds that notonly is the initiation of diarrhea not necessary for decontamination ofthe body, but in preferred embodiments diarrhea is most vehemently to beavoided as part of the detoxification process. This is not only becausediarrhea causes the patient to become dehydrated, but also becausediarrhea may exacerbate serious gastrointestinal disorders such asirritable bowel syndrome (IBS) or Crohn's disease from which somepatients may already suffer.

Furthermore, patients suffering from chronic alcohol dependency oftensuffer from cirrhosis of the liver; both excessive alcohol consumptionand cirrhosis are risk factors in the development of bleeding esophagealvarices, which can quickly become a fatal esophageal hemorrhage.Stimulation of substantial peristaltic movement in the GI tract by theoral ingestion of ascorbic acid in amounts that result in what has beendescribed as “explosive” diarrhea may risk a hemorrhage or bleeding ofbowel or esophageal tissue.

In one example, the method of the invention comprises parenterallyinfusing into a patient a detoxifying composition comprising at least 10g of ascorbic acid, or a salt thereof. As used herein, ascorbic acid maycomprise L-ascorbic acid, R-ascorbic acid and/or racemic ascorbic acid.Ascorbate salts are readily water-soluble ascorbate salts and maycomprise, for example, potassium ascorbate and/or sodium ascorbate.Unless specifically indicated otherwise, the term “ascorbic acid” shallmean one or more of ascorbic acid and an ascorbate salt.

The detoxifying composition may comprise 10 g or more of ascorbic acidor ascorbate salt in solution at a concentration of greater than 0.2grams/ml, and administered at an average rate of at least about 0.5ml/minute. Preferably, the detoxifying composition may comprise at leastabout 25 g ascorbic acid or an ascorbate salt in solution. Preferably,the detoxifying composition may have a concentration of ascorbic acid orascorbate salt of about 0.5 g/ml or more. In presently preferredexamples, the detoxifying composition is parenterally administered at anaverage rate of at least about 1.0 ml/min.

Preferably, the detoxifying composition comprises a local anesthetic.The detoxifying composition may be administered parenterally by hand“push” (e.g., using a syringe) so as to modulate the instantaneous rateat which the composition is administered, such that the instantaneousrate of administration may be momentarily reduced or increased accordingto the patient's comfort level and vital signs.

Preliminary Patient Encounter

Preferably, about 2-4 days prior to performing the methods, andadministering the compositions, of the present invention, information isfirst gathered, and the patient is then started on a preparatory oralregimen, as follows:

A first patient encounter typically includes,

-   -   a) obtaining an extensive medical history and physical        examination from the patient; and    -   b) ordering laboratory tests based on genetic, blood and urine        analysis:

These tests may include:

1) A test for glucose-6-phosphate dehydrogenase (G6PD) enzymedeficiency. The results of this test are essentially a “go/no go”indicator for the suitability of a patient for the methods describedherein.

If a patient is G6PD deficient, their red blood cells lyse easily,leading to hemolytic anemia, and such patients should not be given dosesof ascorbic acid greater than about 500 mg.

2) obtaining genomic testing for single nucleotide polymorphisms (SNP)in the subject's DNA. SNPs are defined as a variation in a singlenucleotide that occurs at a specific position in the genome (generallywithin the coding sequence of a gene), where each variation is presentto some appreciable degree within a population. SNPs can be determinantsfor disease states; diseases such as sickle cell anemia, β-thalassemiaand cystic fibrosis result from SNPs.

SNPs can occur in genes involved in methylation pathways; a well-knownSNP is in the methylene tetrahydrofolate reductase (MTHFR) gene whichnormally breaks down homocystienese variants. Catalogs and databases ofvarious SNPs are well known and widely available. For example, academic,governmental, and private databases exist which list SNPs (see theNational Institutes of Health web pagehttps://www.ncbi.nlm.nih.gov/snp). Additionally, DNA sequence testinglaboratories are widely accessible now, from private testing sites suchas from www.23andme.co. Companies like 23andMe, Inc. also possess SNPdatabases that can be accessed and used to determine whether a givenperson's genome contains any particular identified SNP, and matches sucha person's genome to known genetic alleles contained in the SNPdatabase.

3) blood concentration of the amino acid homocysteine. High levels areassociated with a greater than average risk of heart attack, stroke orblood dots, and levels should be lowered before beginning drugdetoxification therapy.

4) drugs of abuse serum and urine screen.

5) CMP (Complete metabolic panel): This test includes blood tests for:

-   -   glucose, which is the major energy source for the body; a steady        supply must be available for use, and a relatively constant        level of glucose must be maintained in the blood.    -   calcium; essential for the proper functioning of muscles,        nerves, and the heart and is required in blood clotting and in        the formation of bones.    -   serum albumin; produced in the liver and serves as a carrier for        agents such as water, cations such as Ca⁺⁺, Na⁺ and K⁺, fatty        acids, hormones, bilirubin, thyroxine (T4) and drugs (including        barbiturates). Low serum albumen may be caused by liver disease,        nephrotic syndrome, burns, loss of protein from the        gastrointestinal system, malnutrition, late pregnancy, genetic        variations and malignancy. High serum albumin indicates        dehydration.    -   total serum protein.    -   electrolytes (e.g., sodium, potassium, CO₂, chloride).        -   (BUN (blood urea nitrogen) urea; (a nitrogenous compound) is            normally filtered out of the blood by healthy kidneys; high            serum urea is an indicator of kidney malfunction.        -   Creatine; a waste product produced in the muscles; it is            normally filtered out of the blood by the kidneys, so blood            levels are a good indication of how well the kidneys are            working.        -   Liver tests: ALP (alkaline phosphatase)—enzyme found in the            liver and other tissues, bone; elevated levels of ALP in the            blood are most commonly caused by liver disease or bone            disorders; ALT (alanine amino transferase, also called            SGPT)—enzyme found mostly in the cells of the liver and            kidney; a useful test for detecting liver damage; AST            (aspartate amino transferase, also called SGOT)—enzyme found            especially in cells in the heart and liver; also a useful            test for detecting liver damage.

6) CBC (complete blood count)

7) Hepatitis virus panel for hepatitis A virus, hepatitis B virus, andhepatitis C virus).

G₀/N₀ G₀ Decision Point

Based on certain of the results obtained from the blood, urine and DNAtesting (for example, without limitation, a finding of G6PD deficiency;a positive HIV test result; or an active hepatitis infection) a decisionmay be made that a particular patient is not suitable for thedetoxification method if the present invention, either permanently (suchas in the case of G6PD deficiency) or temporarily (such as in the caseof an active hepatitis A infection).

Customizing the Compositions to the Patient

Assuming that the test results fail to indicate that the patient ispresently unsuitable for treatment. In other cases, such as in theidentification and screening of short polynucleotide polymorphisms(SNPs) associated with the methylation or demethylation of compounds orregulatory nucleic acids. Methylation of gene promoter regions is oftenassociated with the suppression of gene transcription in these genes,while demethylation of such regulatory regions may be associated with“up-regulation” of transcription from this gene. In some cases, the SNPdata can provide information permitting the clinician to increase ordecrease the dosage and identities of methylation and methyltransferaseagents (such as S-adenosyl methionine, or SAM-e) and vitamins andminerals that which can aid in promoting liver function and be helpfulin the treatment of depression, atherosclerosis, and osteoarthritis.

Preferably, the patient is seen 3-4 days prior to the first day oftreatment. It is at this time that the personal history is taken, thephysical examination is performed, and the laboratory tests are ordered.Also at this time patient is familiarized with the detoxification methodand program, and given an idea of what to expect during treatment.

After having obtained test results and determined that the patient issuitable for the detoxification treatment and does not haveglucose-6-phosphate dehydrogenase deficiency, the patient is begun on adaily oral regimen of vitamin and mineral supplements, preferably atleast 2-3 days prior to parenteral detoxification.

The oral regimen will typically involve two daily supplement packets: amorning (AM) dose and an evening (PM) dose.

In one embodiment, a first supplement packet may comprise: about 1 gramof ascorbic acid; about 250 mg of B complex vitamins (at least vitaminsB1, B2, B3, B5, B6, B7, B9 and B12); about 400 mg of S-adenosylmethionine (SAM-e); about 400 mg of methyl tetrahydrofolate (MTHF);about 600 mg N-acetyl cysteine (NAC); and about 500 mg tyrosine.

In one embodiment, a second supplement packet may comprise: about 1 gramof ascorbic acid; about 500 mg of glutamine; about 500 mg of GABA(gamma-aminobutyric acid or 4-aminobutanoic acid); about 1 gram oftryptophan; about 100 mg of 5-hydroxy tryptophan; about 5000 units ofVitamin D; about 0.5 mg melatonin; about 2 μg selenium; and about 25 mgzinc.

Some recent research finds GABA accumulation in the synaptic cleft ofthe amygdala to be associated with an inability to internalize GABA bysome post synaptic neurons. See Rainer Spanagel, Abberant ChoiceBehavior in Alcoholism, Science 360:63951298-1299 (Jun. 22, 2018). Thus,in some embodiments of the present invention addition of GABA is avoidedin any oral of parenteral composition.

In other embodiments a single daily oral supplement packet may containany or all of the ingredients of the first supplement packet and/or thesecond supplement packet described above.

In another embodiment the first supplement packet is given a morning(AM) dose.

In another embodiment the second supplement packet is given as anafternoon or evening (PM) dose.

It will be understood that the supplement packets given to each patientmay vary according to the results of the blood, urine and DNA screens.For example, if a particular patient contains SNPs indicating amethylation deficiency, the oral supplements may contain additionalamounts of agents that promote methylation, such as MTHF.

If the screening results indicate toxic amounts of heavy metals, thesupplement packets may be augmented with a chelating agents, such ascalcium disodium ethylene diamine tetraacetic acid (CaNa²EDTA) or thelike.

Similarly, if the test results indicate a particularly high level offree radicals or oxidized species, additional amounts of NAC can begiven to stimulate production of the antioxidant glutathione by thebody.

Melatonin is preferably provided in a PM oral dose to promote sleep.

After starting the patient on the oral supplement packets (about 3-4days prior to beginning the parenteral detoxification treatment) thepatient preferably continues the oral regimen during and between thedetoxification treatments, for about 2 weeks. The oral vitamin andmineral supplement regimen may be discontinued following discharge fromthe detoxification treatment.

The composition is preferably administered parenterally at a rate suchthat 1000 cc are “run” into the patient in about 2 to about 4 hours. Therate can be speeded up if necessary, to control withdrawal symptoms,muscle cramping or spasm, or shakiness.

Below, non-limiting examples are given of formulas for the compositionof this invention.

In another example the method of the invention comprises parenteraladministration of the following compositions:

A) IV Bag 1: which comprises at least about 10 g of ascorbic acid in asubstantially isotonic solution. Preferably, IV Bag 1 also contains:

-   -   one or more vitamin comprising: Vitamin B1 (thiamine), Vitamin        B2 (riboflavin), Vitamin B3 (niacin or nicotinamide), Vitamin B9        (folate or folic acid). Vitamin B5. Vitamin B6, B7 (biotin),        and/or B12;        -   one or more mineral comprising a major mineral such as            soluble calcium (i.e., calcium gluconate), sodium,            potassium, magnesium, phosphorus and sulfur, a trace            mineral, such as iron, zinc, iodine, selenium, copper,            manganese, fluorine, chromium and molybdenum.    -   one or more amino acid comprising taurine and/or threonine.

In one example, IV Bag 1 contains amino acids, but does not contain the20 amino acids used in human protein synthesis. In other examples IV Bag1 contains each of the 20 amino acids used in human protein synthesis.

Vitamin B1 (thiamine) is preferably present in a concentration of fromabout 50 mg to about 80 mg per 100 ml. However, up to a total of about10 g may be administered if necessary to help control tremors. Thiamineis a coenzyme in the catabolism of carbohydrates and amino acids.

Vitamin B3 (niacin (nicotinic acid) or nicotinamide) is preferablypresent in an amount from about 900 mg to about 1500 mg per 100 ml.Vitamin B3 is important in the DNA repair and many metabolic processes,and deficiencies in the form of the disease pellagra, commonly seen inchronic alcoholics, can lead to dementia and death.

Vitamin B5 (pantothenic acid) is present at a preferred amount of from400 mg to about 1200 mg. Vitamin B5 is a precursor of Coenzyme A, whichis involved in fatty acid synthesis and energy production in the citricacid cycle.

Vitamin B6 (Pyridoxine or Pyridoxal-5-Phosphate) (about 100 mg) isassociated with the production of neurotransmitters, and is required foramino acid, carbohydrate and lipid synthesis.

Vitamin B7 (Biotin) (about 10 mg) is a necessary co-factor for manymetabolic enzymes, and a deficiency in biotin can cause highersusceptibility to diabetes and diseases of the skin intestinal tract,and nervous system.

Vitamin B9 (Folate or Folic acid) (about 10 mg) is essential for humangrowth and development, and encourages normal nerve and proper brainfunctioning may help reduce blood levels of the amino acid homocysteine,reducing risks of heart attack.

Vitamin B12 (Cobalamin/Cyanocobalamin) (about 2 mg) affects thedevelopment and maintenance of red blood cells, nerve cells, and normalmyelination (covering) of nerve cells. It also aids in the production ofDNA, RNA, and neurotransmitters.

In one embodiment the IV Bag I is provided in a 500 cc volume as anisotonic parenteral solution. In order to assure the stability of theingredients, the components of IV Bag I are mixed shortly, such as 15minutes, prior to use.

When administration of IV Bag 1 is begun, the patient is very preferablymonitored by pulse, oxygen, electrocardiogram (EKG) and blood pressure.Vital signs are taken every 20 minutes for the first 2 hours, then everyhour thereafter. Urine samples are taken immediately pretreatment, andagain after the first day's treatment.

Typically, after administration of e.g. 50 cc of IV Bag 1, the patientis given an approximately equal volume of a large dose of ascorbic acid(or a water-soluble ascorbate salt) in solution as follows:

B) IV Push 1 (IVP #1)

65 cc of a hypertonic solution containing 25 grams ascorbic acid (or awater-soluble ascorbate salt), 0.5%, by weight of sodium bicarbonate asan alkalizing agent, 1% by weight of lidocaine as a local anesthetic, 5%of calcium gluconate (to treat to treat low blood calcium, high bloodpotassium), and 20% by weight of magnesium chloride.

The high, hypertonic concentration of ascorbic acid administeredfollowing the prior administration of lower concentrations in theisotonic IV 1 solution, is particularly important from a therapeuticperspective.

Very preferably the IV Push 1 is administered manually by a physician orunder physician's supervision so that the patient's vital signs andcomfort level may be monitored and administration may be spread orslowed, as appropriate, based upon the patient's comfort and safety.Preferably the 65 ccs of the IVP 1 is administered at an average rate of1 cc/minute or more such as 1.25 ml/minute or about 1.5 ml/minute, orso.

Ascorbic acid is known to function as a very effective antioxidant atcertain, generally normal to low, concentrations, and may act as anoxidizing agent at other, generally higher/pharmaceuticalconcentrations. Also, ascorbic acid or ascorbate is able to act as an“exciter”, enhancing adrenergic and histaminergic ligand potency throughan extracellular mechanism involving binding of the enhancer to thefirst extracellular loop of the relevant aminergic GPCR. See e.g.,Robert Root-Bernstein & Patrick E. Dillon, A Common Molecular MotifCharacterizes Extracellular Allosteric Enhancers of GPCR AminergicReceptors and Suggests Enhancer Mechanism of Action, C URR. MED. CHEM.21: 3673, 3774 (2014).

in addition to ascorbic acid, several other classes of compounds havealso been characterized as significantly enhancing aminergic GPCRactivity. These compounds include folic acid, ethylenediaminetetraaceticacid (EDTA), opiate drugs and their antagonists, opioid peptides,corticosteroids, members of the citric acid cycle, and variousflavenoids. All of these compounds have been demonstrated to producesignificant (three- to ten-fold) enhancement of the potency and durationof activity of aminergic compounds while having no intrinsic activitythemselves on aminergic systems. See Bernstein & Dillon at 3673.

Once the IVP 1 push dose has been given, the patient is then immediatelygiven the remainder of IV Bag 1 at about 2.5 ml/minute.

IV Push 2 (Glutathione)

Following administration of IV Bag 1, the patient is then given about 20cc of a solution containing about 2 g of glutathione manually in an IVsyringe push over about 2-4 minutes. This will assist the liver byhelping prevent damage to important cellular components caused byreactive oxygen species, such as free radicals, peroxides, lipidperoxides and heavy metals.

IV Bag 2

Following the IV glutathione Push (V Push 2), the patient may then begiven a IV drip of about 50 g ascorbic acid in about 500 cc of waterwith 10 cc of 5% (w) calcium gluconate and 8 cc of 20% (w) magnesiumchloride over about a 2 hour period.

IV Bag #3

Following the administration of IV Bag 2, the patient is then given 500cc of sterile saline over a 1.5 hour period. The patient will becompletely detoxified, even if intoxicated when the treatment wasinitiated, substantially without experiencing withdrawal symptoms,hallucinations, delirium tremens, pain, or other physical symptoms ofdrug or alcohol withdrawal. Maintenance of a healthy diet and continuedrestorative treatments with vitamins and minerals to mend and nourishthe body help create the metal habit required to maintain sobriety oncedetoxification removes the physical discomfort. When sterile saline isused it is preferably a 0.9% normal solution of sodium chloride. Sodiumchloride keeps electrolyte levels of the red blood cells in balance. Itsnormality is selected to be compatible with blood serum, so that, ifinjected, the solution will not appreciably alter the osmolality ofblood serum or cause hemolysis of red blood cells. The saline solutionirrigates the circulatory system and guards against dehydration ifdiarrhea develops.

It is not necessary for the patient to be sober when the first day ofparenteral treatment is given. The patient should eat a good breakfast,and should list food, drink and drugs consumed in the morning prior tothe visit.

In an important embodiment, and while not wishing to be bound by theory.Applicant believes that methods which combine administration ofrelatively low doses of ascorbic acid, such as the doses contained inthe oral supplement packets (which tend to be oxidizing), followed withhigher dose, parenteral administration of ascorbic acid (which tend tobe reducing/antioxidizing) in a hypertonic solution, is able to firstcause the complete oxidation, and thus the “labeling”, of metabolicby-products and toxins for subsequent disposal by the body. Thehypertonic, anti-oxidizing high dose of ascorbic acid will then removefree radicals and cause the reduction of residual oxidizing agents inthe body. The high concentration of the hypertonic ascorbic acid dosewill, by virtue to the high osmotic pressure, cause the ascorbic acid topenetrate cell membranes and be stored within the cells themselves.

Almost invariably, treatment-naive patients suffering from alcohol,opiate, barbiturate, benzodiazepine, or amphetamine addiction who aretreated using the protocol described above display no symptoms of “coldturkey”-type withdrawal, seizures, delirium tremens, vomiting, severemuscle spasms, agitation, lacrimation from the nose and eyes,uncontrollable urination, nausea, and in severe cases, convulsions,respiratory failure, and cardiac arrest.

The treatment is essentially the same for patients suffering fromalcohol dependency and drug dependency. Indeed, today most alcoholicpatients have a drug dependency as well. For alcoholic patients,following the initial detoxification treatment, additional agents may beadded such as a lipotropic formula for reducing triglyceride levels inthe bloodstream. Such a formula may comprise, for example, a lipotropicformula for reducing triglyceride levels in the bloodstream comprisingabout 2500 mg choline bitartrate, about 150 mg betaine hydrochloride,about 15 mg d-calcium pantothenate, and about 750 mg lecithin, in asuitable pharmacological carrier. Additionally the patient may be givena digestive and pancreatic enzyme formula, N,N dimethylglycine, and asupplement of L-glutamine.

The invention is now described with reference to specific examples,which do not limit, but rather expand the scope of the presentinvention.

DETAILED DESCRIPTION

This invention provides a therapeutic detoxifying composition andtreatment method for reducing or eliminating symptoms of drug or alcoholwithdrawal. The method and compositions rapidly detoxify the subjectwhile blocking withdrawal symptoms, while nutritionally restoring thepatient's body from a malnourished state.

Illicit or commonly abused drugs and alcohol may have a high “addictionliability” (defined as a high likelihood (e.g., greater than 20%, orgreater than 30%, or greater than 40%, or greater than 50%, or greaterthan 60% or greater than 70%) that long-term or high dose use will leadto compulsive use) and/or a high “dependence liability” (defined as ahigh likelihood (e.g., greater than 20%, or greater than 30%, or greaterthan 40%, or greater than 50%, or greater than 6% or greater than 70%)that withdrawal symptoms will occur when the SOA use ceases). Thepresent invention is able to treat both addiction liabilities anddependence liabilities.

In addition to alcohol, examples of substances of abuse (SOAs) which arecapable of treatment by this invention include, but are not limited to,heroin, opium, methodone, cocaine, marijuana, LSD, mescaline, peyote,MDA, MDMA (ecstasy) and other psychedelics, PCP, barbiturates, tobacco,amphetamines (including methamphetamine), benzodiazepines such asValium™, Librium™ and Klonopin™), and other prescription ornon-prescription drugs or medications, or toxic chemicals. Presently, itappears that this invention is capable oft detoxifying any substancefrom the human body within a 6-8 hour period.

While not wishing to be limited by theory, Applicant believes that thepresent methods and compositions work by a combination of mechanisms.Vitamin C (ascorbic acid) competes with the SOA and toxic or deleteriousmetabolites at the cell surface and internal receptors, such as the NMDAglutamate neuroreceptor and the μ opioid receptor. The highconcentrations of Vitamin C used in the present method detaches suchcompounds and blocks their reattachment to the receptor(s).

Such high concentrations of ascorbic acid also permit the intracellularaccumulation of ascorbic acid. Such accumulation appears to befacilitated by high affinity, high specificity binding to a proteinnamed SVCT2, and perhaps also by the transport protein SVCT1.

At low concentrations of ascorbic acid, free radicals and reactiveoxidative species (ROS) are reduced by the antioxidant activity ofascorbic acid. At high concentrations of ascorbic acid, in whichascorbic acid acts as a pro-oxidant, other reactive oxidative speciesmay be further oxidized to increase reactivity, then neutralized by aless reactive antioxidant to neutrality.

Ascorbic acid also detoxifies inflammatory and environmental toxins,such as organic phosphates and plastics, which can cause anxiety anddepression if untreated.

Finally, the methods and compositions of the present invention restorenutritional health to the individual being treated. These changes arereinforced by instruction in modifications to the patient's diet andlifestyle.

Further disclosure is provided in the example provided below, whichillustrates, but does not define the invention; the invention beingdefined solely by the claims which conclude this specification.

EXAMPLE

A female patient is 32 years old and is addicted to heroin, which shehas been using for 2 years, after developing a dependence onprescription opiates.

First Patient Encounter

An extensive patient medical history is taken, and a physicalexamination conducted. The patient presents as than and somewhatundernourished, but otherwise in good health. The patient states thatshe is under the influence of heroin, having injected the drugapproximately one hour previously. DNA (e.g. 23 and me), blood and urineis taken, and lab tests ordered for SNPs, homocysteine. Brain DerivedNeurotrophic Factor (BDNF), cortisol, DHEA, ACTH, ceruloplasmin, copper,zinc, iron, selenium. Vitamins B-1, B-3, B-5, B-6, B-7, B-9 & B-12,glyphosate, a screen for common drugs of abuse in blood and urine, G6PD,CMP, CC, hepatitis panel (A, B and C)), and an HIV test.

The patient is provided with oral supplements comprising morning (AM)and evening (PM) packages, which are buffered to physiological pH.Patient will take oral supplements from this first encounter until oneday following discharge; approximately 2 weeks.

The AM Package comprises:

Ascorbic Acid   1 gram Super B complex vitamins 250 mg SAM-e(S-adenosylmethionine) 400 mg MTHF 100 mg NAC 600 mg Tyrosine 500 mg

The PM Package comprises:

Ascorbic Acid 1 gram Glutamine 500 mg GABA 500 mgTryptophan/5-hydroxytryptophan 1000 mg (Tryp)/100 mg (5-HTP) (5-HTP)Vitamin D 5000 units Melatonin 0.5 mg Selenium/Zinc 2 μg (Se)/25 mg (Zn)

The initial detox treatment is scheduled within 3 to 4 days after theinitial patient encounter. During this time the test resub are obtainedand analyzed. The patient is found not to be G6PD deficient, or positivefor IV or hepatitis A, B or C. During this time between the first andsecond Patient Encounter (first day of treatment) the oral dose ofascorbic acid preferably increased from 1 gram twice a day to 2 gramsper day over the 3 to 4 day time interval.

The patient is provided a light breakfast of fruit and coffee, and urineis taken prior to treatment. The patient indicates that she has injecteda dose of heroin earlier in the morning.

The following ingredients were mixed approximately 1 hour prior totreatment; it will be understood that minor variation in the amounts ofthese ingredients is permitted and falls within the cope of theinvention:

IV BAG #1 Ascorbic Acid 10 grams Taurine 250 mg Threonine 100 mg ZincSulfate 3 mg Selenium (Sodium Selenite) 200 mcg Trace minerals 2 mlPotassium chloride 4 meq Calcium gluconate 50-75 mg Vitamin B6 100 mgVitamin B5 250 mg Folic Acid 10 mg Thiamine 100 mg Nicotinamide 100 mgSterile Water for infusion q.s. to 500 cc

IVP #1 (Syringe “Push” #1) Ascorbic Acid (50% (w) soln) 25 grams (50cc); final 36%(w) Sodium bicarbonate (8.5%(w) soln) 10 cc; final 1.2%(w) Lidocaine (1%(w) soln) 0.5 cc; final 0.0072% (w) Calcium gluconate(5% (w) soln) 2.5 cc; final 0.14% (w) Magnesium chloride (20% (w) soln)2.5 cc; final 0.57% (w)

The hypotonic aqueous solution IVP #1 is loaded into a syringe inpreparation for use.

The patient is made comfortable on a reclining chair, and vital signs(e.g., heart rate, respiration rate, blood pressure, blood O₂,temperature) are monitored every 20 minutes for the first two hours (andduring “push” procedures), then hourly during the remainder of theprocedure. The patient is encouraged to relax, and is offered readingmaterial and headphones playing soothing music as a relaxation aid.After about 20 minutes, the patient indicates she is experiencingneither any sensation of being under the influence of heroin nor anycraving for heroin or discomfort, such as withdrawal symptoms,associated with the discontinuation of the use of heroin.

The contents of IV Bag #1 (an isotonic solution) are startedintravenously, at a rate of about 2.5 ml/minute. After 15-20 minutes(i.e., after about 50 cc of IV Bag #1 have been administered), theinfusion of IV Bag #1 is stopped, and IVP #1 is administered manuallyusing the syringe at an average rate of about 2.3 ml/min. This rate canbe speeded or slowed, as necessary, depending on the patient's comfortlevel. The IVP #1 solution s quite dense, and the patient may experiencesome minor pain or discomfort during the “push” procedureadministration. Vital signs are monitored while the IVP #1 solution isinjected manually. The lidocaine added to IVP #1 renders the degree ofdiscomfort reported by the patient during this process minimal.

Following administration of IVP #1 (about 30 minutes), the patient isadministered the remainder of IP Bag 1 at an infusion rate of about 2.5ml/min. Following administration of IVP #1 the patient shows no signs ofheroin intoxication, and no withdrawal symptoms. The patient reports nowithdrawal symptoms or related discomfort and no craving for heroin.

During administration of IV Bag 1, a fresh aqueous solution labeled IVP#2 is made, consisting of 20 cc of 10% (w) glutathione. Additionally. IVBag #2 is also made up in advance, comprising 500 cc of an aqueoussterile solution containing 50 g ascorbic acid, 10 cc of 5% (w) calciumgluconate, and 5 cc of 20% (w) magnesium chloride.

Following administration of the remainder of IV Bag #1, the 20 cc IVP #2solution is loaded into a syringe and manually adminstered within a timeperiod of 2-10 minutes; preferably within about 2 to about 6 minutes, orwithin about 2 to about 4 minutes. As with IVP #1, the patient ismonitored during the IVP #2 administration, and the rate ofadministration is slowed if the patient experiences any discomfort.Glutathione is a major and highly conserved anti-oxidant in plants,animals, fungi, bacterial and some archaea, and is capable of preventingdamage to important cellular components caused by reactive oxygenspecies such as free radicals, peroxides, lipid peroxides, and heavymetals.

Following administration of IVP #2 IV Bag #2 is administered over a2-hour period of time (i.e., at an average rate of about 4 ml/min. This500 cc IV Bag #2 contains 0% (w) ascorbic acid, as well as calcium andmagnesium for cardiac and nervous system health.

Finally, TV Bag #3 (sterile isotonic saline solution) is administered atabout the same rate (about 500 cc over a 2 hour period) to clear out theneutralized reactive oxidative species and metabolic by-products.

Following the procedure, a urine sample is taken before the patientleaves the facility, and the patient is then sent home with orders todrink plenty of fluids, to rest and to refrain from drinking or usingdrugs. The patient at this point should be placed in a sober livingenvironment, and receive psychological counseling and/or attend 12 stepmeetings to reinforce the physical detoxification, which is wellunderway at the end of the first detoxification treatment.

Third Patient Encounter (Day After Initial Detox)

Urine is collected before the IV treatment. IV treatment is simply 500cc t) 1000 cc of sterile saline, administered at a rate of about 250 ccper hour. Urine is again collected after the IV treatment. The urinesamples are collected to monitor substances of abuse and theirmetabolites. The urine samples will reveal not only the presence orabsence or reported drug (including alcohol) but any unreported drugs,such as nicotine.

Fourth Patient Encounter (Third Day Following Initial Detox)

Urine is collected before the IV treatment. IV treatment is identical tothat of the Second Patient Encounter, except that IV Push #1 is notadministered. Thus, IV Bag 1 is administered, followed by IVP #2, andthen IV Bag 2 and IV Bag 3. The administration and flow rates of the IVBags and IV push #2 are the same as in the Second Patient Encounter.Urine is again collected after the IV treatment.

Following the Fourth Patient Encounter on days 4-9, the patient is notseen, but is referred to a sober living environment, with healthy,“paleo” diet-type meals (i.e., no processed foods, no starches orprocessed meats, fresh vegetables, fruits, whole nuts and grins.

Fifth Patient Encounter (Tenth Day Following Initial Detox)

Urine is collected before the IV treatment. IV treatment is identical tothat of the Second Patient Encounter, except that IV Push #1 is notAdministered. Thus, IV Bag 1 is administered, followed by IVP #2, andthen TV Bag 2 and IV Bag 3. The administration and tow rates of the IVBags and TV Push #2 are the same as in the Second Patient Encounter.Urine is again collected after the TV treatment.

Blood samples are then taken for labs showing: hormone levels (e.g.,ACTH (Adrenocortictropic hormone), cortisol, testosterone,dihydrotestosterone, DHEA, estrogens, thyroid hormones), homocysteinelevels, CBC, CMP, (GT (gamma-glutamyltransferase) test of liverfunction), lactic acid dehydrogenase (LDH) test of cellular damage andkidney and liver disease, triiodothyronine (13) test (thyroid function),Reverse T3 test (to eliminate a diagnosis of hyperthyroidism),thyroid-stimulating hormone (TSH) test, lipase/amylase tests ofpancreatic function. WHAT FURTHER ACTIONS (IF ANY) ARE TAKEN BASED ONTHE RESULTS OF THESE TESTS? Ref #8

Assuming these tests confirm the restoration of the patient's basicnutritional health, the patient has now completed the detoxificationregimen, without withdrawal symptoms and without craving for heroin. Thepatient continues to obtain psychological counseling and to attend 12step meetings to reinforce her transition from a drug-using life to adrug-free life.

Other aspects and embodiments of the invention will be apparent from theclaims that follow this specification. To the extent that a plurality ofinventions may be disclosed herein, any such invention shall beunderstood to have been disclosed herein alone, in combination withother features or inventions disclosed herein, or lacking any feature orfeatures not explicitly disclosed as essential for that invention. Forexample, the inventions described in this specification can be practicedwithin elements of, or in combination with, any other features,elements, methods or structures described herein. Additionally, featuresillustrated herein as being present in a particular example areintended, in other examples of the present invention, to be explicitlylacking from the invention, or combinable with features describedelsewhere in this patent application, in a manner not otherwiseillustrated in this patent application or present in that particularexample. The scope of the invention shall be determined solely by thelanguage of the claims.

Thus it will be understood that the various descriptions of theinvention provided herein illustrate presently preferred examples of theinvention, but that the invention is not limited to the examplesprovided, or to the specific configurations and relation of elementsunless the claims specifically indicate otherwise. Based upon thepresent disclosure a person of ordinary skill in the art willimmediately conceive of other alternatives to the specific examplesgiven, such that the present disclosure will be understood to provide afull written description of each of such alternatives as if each hadbeen specifically described.

What is claimed:
 1. A method for attenuating symptoms of withdrawal todrugs or alcohol in a patient, comprising parenterally administering tosaid patient a solution containing 10 g or more of ascorbic acid at aconcentration of 0.2 g/ml or greater, and an alkalinizing agent.
 2. Themethod of claim 1 wherein said solution contains 15 g or more ofascorbic acid.
 3. The method of claim 1 wherein said solution contains20 g or more of ascorbic acid.
 4. The method of claim 1 wherein saidsolution contains 25 g or more of ascorbic acid.
 5. The method of claim1 wherein said solution has an ascorbic acid concentration of at least0.5 g/ml.
 6. The method of claim 1 wherein said solution is parenterallyadministered at a rate of at least about 1.0 ml/min.
 7. A method forattenuating symptoms of withdrawal to drugs or alcohol in a patient,comprising parenterally administering to said patient: a) a dose of ahypertonic solution comprising about 10 g or more of ascorbic acid at aconcentration of 0.2 g/ml or greater, and an alkalinizing agent; and b)a dose of a substantially isotonic saline solution.
 8. The method ofclaim 7 further comprising the step: c) parenterally administering asolution comprising about 2 g glutathione at a concentration of about0.1 g/ml.
 9. The method of claim 7 wherein said solution comprisesascorbic acid at a concentration greater than 0.2 g/ml.
 10. The methodof claim 7 wherein said solution comprises at least 20 g ascorbic acid.11. The method of claim 10 wherein said solution comprises ascorbic acidat a concentration greater than 0.2 g/ml.
 12. A method for attenuatingsymptoms of withdrawal to drugs or alcohol, comprising administeringparenterally administering to a subject in need thereof a hypertonicsolution comprising about 10 g or more of ascorbic acid at aconcentration of about 0.2 grams/ml or more, and an alkalinizing agent.13. The method of claim 12 in which the amount of ascorbic acid is about20 g or more.
 14. The method of claim 13 in which the amount of ascorbicacid is about 25 g or more.
 15. The method of claim 12 wherein thepatient is parenterally administered a first solution containing about2% (w) ascorbic acid immediately before the hypotonic solution isparenterally administered.
 16. The method of claim 12 wherein, followingadministration of the second solution, a third solution containing about2 g of glutathione is manually parenterally administered.
 17. The methodof claim 16 comprising parenterally administering a fourth solutioncontaining about 2% (w) ascorbic acid.
 18. The method of claim 12wherein at least one of said solutions contains Vitamin B5, Vitamin B6,thiamine, and amino acids.
 19. The method of claim 12 wherein thehypertonic solution comprises ascorbic acid at a concentration greaterthan 0.2 grams/ml.